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A recent high-density linkage screen confirmed that the HLA complex contains the strongest genetic factor for the risk of multiple sclerosis (MS). In parallel, a linkage disequilibrium analysis using 650 single nucleotide polymorphisms (SNP) markers of the HLA complex mapped the entire genetic effect to the  HLA-DR-DQ  subregion, reflected by the well-established risk haplotype  HLA-DRB1*15,DQB1*06 . Contrary to this, in a cohort of 1,084 MS patients and 1,347 controls, we show that the  HLA-A  gene confers an  HLA-DRB1  independent influence on the risk of MS (P = 8.4×10 −10 ). This supports the opposing view, that genes in the HLA class I region indeed exert an additional influence on the risk of MS, and confirms that the class I allele  HLA-A*02  is negatively associated with the risk of MS (OR = 0.63, P = 7×10 −12 ) not explained by linkage disequilibrium with class II. The combination of  HLA-A  and  HLA-DRB1  alleles, as represented by  HLA-A*02  and  HLA-DRB1*15 , was found to influence the risk of MS 23-fold. These findings imply complex autoimmune mechanisms involving both the regulatory and the effector arms of the immune system in the triggering of MS.

HLA-A Confers an HLA-DRB1 Independent Influence on the Risk of Multiple Sclerosis